Herpes and other viruses that attack the nervous system may thrive by disrupting cell function in order to hijack a neuron's internal transportation network and spread to other cells.
Princeton University researchers made the first observation in neurons that common strains of the herpes virus indirectly take control of a cell's mitochondria, the mobile organelles that regulate a cell's energy supply, communication with other cells, and self-destruction response to infection. The team reports in the journal Cell Host and Microbe that viral infection elevates neuron activity, as well as the cell's level of calcium a key chemical in cell communication and brings mitochondrial motion to a halt in the cell's axon, which connects to and allows communication with other neurons.
The authors propose that the viruses then commandeer the proteins that mitochondria typically use to move about the cell. The pathogens can then freely travel and reproduce within the infected neuron and more easily spread to uninfected cells. When the researchers made the mitochondria less sensitive to calcium the viruses could not spread as quickly or easily.
These findings reveal a previously unknown and highly efficient mechanism that some of the most common strains of herpes viruses in humans may use to proliferate in the nervous system, said lead author Tal Kramer, a doctoral student in the lab of the paper's co-author Lynn Enquist, the Henry L. Hillman Professor of Molecular Biology and chair of Princeton's molecular biology department.
Kramer and Enquist used rat neurons to study two herpes viruses in the alpha-herpes virus subfamily: pseudorabies virus (PRV), a model alpha-herpes virus that infects animals, and herpes simplex virus 1 (HSV-1), an extremely common human virus that causes cold sores and other lesions. Other human alpha-herpes viruses are responsible for causing diseases such as chicken pox and shingles.
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